We propose to continue our clinical investigation of CAH which consists of a family of disorders of inherited enzymatic defects of adrenal steroidogenesis. We shall concentrate on the defect of steroid 21-hydroxylation and describe the hormonal and genetic basis for the clinical spectrum of virilization. The hormonal studies will distinguish the function of the fasciculata and glomerulosa in the 21-hydroxylase defect to examine the basis for salt-wasting and non-salt-wasting forms of CAH due to 21-hydrox-ylase deficiency. We will study gonadal function in patients with 21-hydroxylase deficiency. Pilot studies to demonstrate the feasibility of screening for CAH will be continued. Finally, we will study aldosterone regulation in CAH due to 21-hydroxylase deficiency and in dexamethasone suppressible hyperaldosteronism. These studies will provide a rational basis for genetic counselling and will also provide improved criteria for diagnosis and treatment of various forms of steriod 21-hydroxylase deficiency so that growth and puberty can proceed normally in these patients.